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      Biological Activity of Berberine—A Summary Update

      review-article
      Author(s): 1 , * , 2 , 1
      Publication date (Electronic):
      Journal: Toxins
      Publisher: MDPI
      Keywords: berberine, anticancer, metabolic syndrome, apoptosis, clinical trials, bioavailability

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          Abstract

          Berberine is a plant metabolite belonging to the group of isoquinoline alkaloids with strong biological and pharmacological activity. Currently, berberine is receiving considerable interest due to its anticancer activity based on many biochemical pathways, especially its proapoptotic and anti-inflammatory activity. Therefore, the growing number of papers on berberine demands summarizing the knowledge and research trends. The efficacy of berberine in breast and colon cancers seems to be the most promising aspect. Many papers focus on novel therapeutic strategies based on new formulations or search for new active derivatives. The activity of berberine is very important as regards sensitization and support of anticancer therapy in combination with well-known but in some cases inefficient therapeutics. Currently, the compound is being assessed in many important clinical trials and is one of the most promising and intensively examined natural agents.

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          Most cited references132

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          Roles of matrix metalloproteinases in cancer progression and their pharmacological targeting.

          Chrisostomi Gialeli, Achilleas Theocharis, Nikos K Karamanos (2011)
          Matrix metalloproteinases (MMPs) consist of a multigene family of zinc-dependent extracellular matrix (ECM) remodeling endopeptidases implicated in pathological processes, such as carcinogenesis. In this regard, their activity plays a pivotal role in tumor growth and the multistep processes of invasion and metastasis, including proteolytic degradation of ECM, alteration of the cell-cell and cell-ECM interactions, migration and angiogenesis. The underlying premise of the current minireview is that MMPs are able to proteolytically process substrates in the extracellular milieu and, in so doing, promote tumor progression. However, certain members of the MMP family exert contradicting roles at different stages during cancer progression, depending among other factors on the tumor stage, tumor site, enzyme localization and substrate profile. MMPs are therefore amenable to therapeutic intervention by synthetic and natural inhibitors, providing perspectives for future studies. Multiple therapeutic agents, called matrix metalloproteinase inhibitors (MMPIs) have been developed to target MMPs, attempting to control their enzymatic activity. Even though clinical trials with these compounds do not show the expected results in most cases, the field of MMPIs is ongoing. This minireview critically evaluates the role of MMPs in relation to cancer progression, and highlights the challenges, as well as future prospects, for the design, development and efficacy of MMPIs. © 2010 The Authors Journal compilation © 2010 FEBS.
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            TGFbeta in Cancer.

            Joan Massagué (2008)
            The transforming growth factor beta (TGFbeta) signaling pathway is a key player in metazoan biology, and its misregulation can result in tumor development. The regulatory cytokine TGFbeta exerts tumor-suppressive effects that cancer cells must elude for malignant evolution. Yet, paradoxically, TGFbeta also modulates processes such as cell invasion, immune regulation, and microenvironment modification that cancer cells may exploit to their advantage. Consequently, the output of a TGFbeta response is highly contextual throughout development, across different tissues, and also in cancer. The mechanistic basis and clinical relevance of TGFbeta's role in cancer is becoming increasingly clear, paving the way for a better understanding of the complexity and therapeutic potential of this pathway.
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              Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor.

              Anne Brunet, Azad Bonni, Michael Zigmond … (1999)
              Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/ threonine kinase Akt, which then phosphorylates and inactivates components of the apoptotic machinery, including BAD and Caspase 9. In this study, we demonstrate that Akt also regulates the activity of FKHRL1, a member of the Forkhead family of transcription factors. In the presence of survival factors, Akt phosphorylates FKHRL1, leading to FKHRL1's association with 14-3-3 proteins and FKHRL1's retention in the cytoplasm. Survival factor withdrawal leads to FKHRL1 dephosphorylation, nuclear translocation, and target gene activation. Within the nucleus, FKHRL1 triggers apoptosis most likely by inducing the expression of genes that are critical for cell death, such as the Fas ligand gene.
              Article 0 comments Cited 391 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Toxins (Basel)
                Journal ID (iso-abbrev): Toxins (Basel)
                Journal ID (publisher-id): toxins
                Title: Toxins
                Publisher: MDPI
                ISSN (Electronic): 2072-6651
                Publication date (Electronic): 12 November 2020
                Publication date Collection: November 2020
                Volume: 12
                Issue: 11
                Electronic Location Identifier: 713
                Affiliations
                [1 ]Chair and Department of Pharmaceutical Botany, Medical University of Lublin, 1 Chodźki St., 20-093 Lublin, Poland; renatanowak@ 123456umlub.pl
                [2 ]Department of Biochemistry, Institute of Medical Sciences, Medical College of Rzeszów University, 16c Rejtana St., 35-959 Rzeszów, Poland; rpodgorski@ 123456ur.edu.pl
                Author notes
                [* ]Correspondence: anna.ochagn@ 123456wp.pl ; Tel.: +48-(50)-4050167
                Author information
                https://orcid.org/0000-0002-1707-9478
                https://orcid.org/0000-0002-7565-7184
                Article
                Publisher ID: toxins-12-00713
                DOI: 10.3390/toxins12110713
                PMC ID: 7697704
                PubMed ID: 33198257
                SO-VID: 02596dbc-5f61-446d-99f0-4f497faf6a20
                Copyright © © 2020 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 02 November 2020
                Date accepted : 10 November 2020
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: berberine,anticancer,metabolic syndrome,apoptosis,clinical trials,bioavailability
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: berberine, anticancer, metabolic syndrome, apoptosis, clinical trials, bioavailability

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